ライフサイエンスコーパス: endocrine

1 nal modification that is known to hamper OCN endocrine action.

2 id, tributyltin, and butylhydroxytoluene, in endocrine-active human-induced pluripotent stem cell-der

3 or during ozonation, agonistic/antagonistic endocrine activities, mutagenic/genotoxic activities, cy

4 s an endogenous hormone with vasopressor and endocrine activities.

5 h can be used to screen potential cumulative endocrine activity in drinking water and to inform prior

6 e diverse biological data for evaluating the endocrine activity of chemicals.

7 6.3 (renal) weeks, and with the exclusion of endocrine AEs, median time to resolution from onset rang

8 traditionally has been thought to depend on endocrine and autocrine/paracrine modulators.

9 and quantifications indicated that exocrine, endocrine and ductal compartments retained the normal pr

10 ineages, we also identify numerous unipotent endocrine and ducto-endocrine bipotent clones.

11 s during pancreas development is critical to endocrine and exocrine cell fate.

12 protein-based tools to correlate behavioral, endocrine and gender traits with hypothalamic neuron ide

13 n optimal biological function, including the endocrine and immune systems.

14 onchial epithelium with KL functioning as an endocrine and local anti-inflammatory mediator that anta

15 anxiety-like behavior, glucose homeostasis, endocrine and molecular markers of insulin resistance, a

16 effects of such compounds on developing gut endocrine and neuroendocrine systems.

17 ward-driven responding, thereby highlighting endocrine and neuropeptidergic signaling in hippocampal

18 e DMH, a structure that modulates autonomic, endocrine, and behavioral responses and is a potential t

19 consisted mainly of skin, gastrointestinal, endocrine, and hepatic immune-related adverse events.

20 ents) were most frequently skin related, GI, endocrine, and hepatic; grade 3 to 4 select AEs occurred

21 AAs cause toxicity to the liver, the immune, endocrine, and male reproductive systems, and the develo

22 onal disorder characterized by reproductive, endocrine, and metabolic abnormalities.

23 We investigated mineral, endocrine, and renal responses during the first 4 hours

24 plications for deciphering potent early-life endocrine, as well as potential gut microbiota impacts o

25 , which is an important neurotransmitter and endocrine, autocrine and paracrine hormone.

26 ips among the brain and the functions of the endocrine, autonomic, and immune systems.

27 s, demonstrating a framework for identifying endocrine bioactive chemicals.

28 throughput data as a health-based screen for endocrine bioactivity of chemicals in water.

29 guidelines and many have been shown to have endocrine bioactivity.

30 e concentrations of many cardiometabolic and endocrine biomarkers.

31 ntify numerous unipotent endocrine and ducto-endocrine bipotent clones.

32 in pancreatic progenitors results in reduced endocrine cell area at birth due to impaired endocrine c

33 expression during late stages of pancreatic endocrine cell development.

34 f Pax4 opened new avenues of research in the endocrine cell differentiation and diabetes fields.

35 endocrine cell area at birth due to impaired endocrine cell differentiation and reduced prenatal prol

36 3 (Ngn3) plays a critical role in pancreatic endocrine cell differentiation, although regulation of N

37 roper induction of NEUROG3 and initiation of endocrine cell differentiation.

38 tly different from humans, canine pancreatic endocrine cell distribution is more similar.

39 s express NEUROG3 but do not adopt alternate endocrine cell fates.

40 NEUROG3, is an essential variable in normal endocrine cell genesis.

41 nto embryonic fates or adopt alternate islet endocrine cell identities.

42 ing genes that specify the alternative islet endocrine cell lineages.

43 -cell dedifferentiation, and not necessarily endocrine cell loss, constitutes a major cause of beta-c

44 morphogenesis, which subsequently determines endocrine cell mass.

45 s and bihormonal cells that displayed hybrid endocrine cell morphological characteristics.

46 YAP stabilisation and endocrine cell specification rely on Galphai subunits, r

47 Many terminally differentiated endocrine cell types, however, remain enriched for LDB1,

48 rine progenitors, regardless of the specific endocrine cell-type chosen.

49 ogenic activity of the stem cells and in the endocrine-cell progenitors differentiating into enteroen

50 natally, an increase in the proliferation of endocrine cells also participates in their expansion.

51 We identified 118 alpha, 105 beta, 6 delta endocrine cells and 47 exocrine cells.

52 n secretory granules which store hormones in endocrine cells and release them upon cell stimulation.

53 ally, in vitro differentiation of pancreatic endocrine cells derived from human pluripotent stem cell

54 We find that islet endocrine cells from older donors display increased leve

55 Deletion of Mtor in pancreatic endocrine cells had no significant effect on their embry

56 nt activation of MAP kinases in neuronal and endocrine cells is critical for cell differentiation and

57 on of the recipients and failed to reach the endocrine cells of grafted islets.

58 er 2 (KCC2, Slc12a5) is expressed in several endocrine cells of the pancreatic islet, including gluca

59 gests that ghrelin, a peptide synthesized by endocrine cells of the stomach and a key component of th

60 ches (termed periphery), produces most islet endocrine cells.

61 novel mutational signature in healthy aging endocrine cells.

62 activating other MAP kinases in neuronal and endocrine cells.

63 iate or become reprogrammed into other islet endocrine cells.

64 define the relative importance of renal and endocrine changes in tenofovir disoproxil fumarate (TDF)

65 anscriptional profiling at E9.5 reveals that endocrine-committed cells are molecularly distinct, wher

66 signal honesty could be based on the shared endocrine control of queen fertility and the production

67 d queen signal production being under shared endocrine control.

68 neral pattern of effects was observed across endocrine (cortisol and testosterone), psychological (fe

69 , theoretically, to prevent survival of both endocrine-dependent and -independent ER+ tumors.

70 zation, followed by validation in the parent endocrine-dependent cell line (MCF-7:WS8), in 2D and 3D

71 endocrine disrupting chemicals during fetal endocrine development may lead to disruption of metaboli

72 ory mechanisms involving the reactivation of endocrine developmental processes that result in dramati

73 3 controls its ability to promote pancreatic endocrine differentiation and to maintain beta cell func

74 a subset of the GP2(+) population undergoes endocrine differentiation by down-regulating GP2 and CD1

75 could be manipulated to promote and maintain endocrine differentiation in vitro and in vivo.

76 f acinar differentiation around E11.5, while endocrine differentiation is proportionally decreased.

77 nd CD142 and turning on NEUROG3, a marker of endocrine differentiation.

78 yperlipidemia (29.2%, 22.1%, and 49.6%), and endocrine disease (21.8%, 27.2%, and 54.0%) were the mos

79 ovascular, neurologic, gastrointestinal, and endocrine disease; cognitive function; serum nutrient le

80 l hypothyroidism is the most common neonatal endocrine disorder and is primarily caused by developmen

81 Primary hyperparathyroidism is an endocrine disorder characterized by autonomous productio

82 Cushing's disease is a rare debilitating endocrine disorder for which few prospective interventio

83 ystic ovary syndrome (PCOS), the most common endocrine disorder of reproductive age women.

84 ent cell replacement for a broad spectrum of endocrine disorders and other organ dysfunctions.

85 y to predict large-scale mixture effects for endocrine disrupters with a predictive toxicology approa

86 ion for monitoring waters for chemicals with endocrine disrupting activity.

87 Blocking NF-kappaB rescues endocrine disrupting chemical-induced aberrant mitochond

88 ive adjuvant, the impact of these estrogenic endocrine disrupting chemicals (EDCs) on the immune syst

89 Persistent exposure to man-made endocrine disrupting chemicals during fetal endocrine de

90 to demonstrate adverse impacts of obesogenic endocrine disrupting chemicals in the developing endocri

91 hysiological low-dose exposure to ubiquitous endocrine disrupting chemicals including, perfluoro-octa

92 Endocrine disrupting chemicals induce endoplasmic reticu

93 Many endocrine disrupting chemicals, including bisphenol-A (B

94 Assessing how endocrine disrupting compounds (EDCs) affect population

95 erature increases may affect the activity of endocrine disrupting compounds (EDCs), particularly in s

96 An endocrine disrupting effect of C47 was observed already

97 er bisphenol-A, a prominent contaminant with endocrine-disrupting capabilities, altered susceptibilit

98 of environmental chemicals with potentially endocrine-disrupting capabilities.

99 exposure to bisphenol A (BPA), a ubiquitous endocrine-disrupting chemical, is associated with advers

100 he risks of perchlorate-a well-characterized endocrine-disrupting chemical-to vulnerable populations

101 There are a number of known sources of endocrine-disrupting chemicals (EDCs) and other hazardou

102 Endocrine-disrupting chemicals (EDCs) are suspected of a

103 A growing body of evidence links endocrine-disrupting chemicals (EDCs) with obesity-relat

104 Endocrine-disrupting chemicals such as p,p'-dichlorodiph

105 es in animals have demonstrated that ATZ has endocrine-disrupting effects on male and female reproduc

106 ith pubertal development are consistent with endocrine-disrupting effects.

107 d in the European market as a substitute for endocrine-disrupting phthalates.

108 S), an antimicrobial chemical with potential endocrine-disrupting properties, may pose a risk to earl

109 re available for other phenols with possible endocrine-disrupting properties.

110 HIV-seronegative young men and suggest that endocrine disruption (PTH-FGF23) is a primary contributo

111 are investigated when interpreting putative endocrine disruption in Arctic wildlife with potential p

112 yolk precursor, is a well-known biomarker of endocrine disruption in oviparous vertebrates.

113 CPC's effects on mitochondrial toxicity and endocrine disruption in vitro.

114 The primary mechanism is endocrine disruption of the binding affinity for the est

115 to biotransformation, oxidative stress, and endocrine disruption were also measured using quantitati

116 of interest such as acute systemic toxicity, endocrine disruption, skin sensitization, and many other

117 has been implicated in neurodevelopment and endocrine disruption, with expected metabolism perturbat

118 nked to cancer, neurological impairment, and endocrine disruption.

119 a TH-controlled metamorphosis, sensitive to endocrine disruption.

120 isphenol A (BPA), a widespread environmental endocrine disruptor and putative obesogen.

121 ns unknown whether ibuprofen could act as an endocrine disruptor as reported for fellow analgesics pa

122 The endocrine disruptor bisphenol A (BPA) and the pharmaceut

123 Exposure to the environmental endocrine disruptor bisphenol A (BPA) is ubiquitous and

124 through the electrochemical detection of the endocrine disruptor bisphenol A, as well as the capture

125 The suspected endocrine disruptor BP-3 has been detected in the air an

126 Bisphenol A (BPA) is an endocrine disruptor frequently detected in human bioflui

127 inducer of recombination, but an established endocrine disruptor with mixed agonist/antagonist activi

128 relevant concentrations of commonly detected endocrine disruptors in a model vertebrate species.

129 ce presented by experts at the First African Endocrine Disruptors meeting.

130 approach to estimate sex-specific effects of endocrine disruptors on health.

131 ly according to sex, as is often the case in endocrine disruptors research, investigators routinely e

132 triclocarban are environmentally persistent endocrine disruptors that bioaccumulate in and are toxic

133 s composed of fluorescent and nonfluorescent endocrine disruptors were analyzed.

134 Many pollutants are endocrine disruptors with impacts on reproduction and he

135 Phthalates and bisphenol A (BPA) are endocrine disruptors, and previous research has suggeste

136 sure, and structural similarities with known endocrine disruptors, concerns have been raised regardin

137 hin first trimester, ibuprofen causes direct endocrine disturbances in the human fetal testis and alt

138 ously proliferate and differentiate into the endocrine, ductal and acinar lineages.

139 nduced aberrant mitochondrial phenotypes and endocrine dysregulation, but not ER-stress and p53-phosp

140 d allow examination of hypotheses concerning endocrine effects from dietary compounds.

141 were located in the insulitic lesion in the endocrine-exocrine interface.

142 to investigate the relationship of GWG with endocrine factors such as adiponectin, leptin, and C-rea

143 s activity is modulated by neuropeptides and endocrine factors.

144 ent murine beta cells acquired non-beta cell endocrine features, resulting in populations of complete

145 tant feature in the temporal coordination of endocrine function and gene expression.

146 rostin, these findings suggest an unexplored endocrine function for sclerostin that facilitates commu

147 Moreover, endocrine function was recovered in ovariectomized recip

148 tify furin as an important regulator of bone endocrine function.

149 mouse models of type 2 diabetes, suggest an endocrine function.

150 To compare neurocognitive and endocrine functional outcomes and survival at 5 years in

151 also continual repression of closely related endocrine gene programs.

152 es in H3K27me3, at the promoters of affected endocrine genes.

153 stinal system (GI), followed by the bronchi, endocrine glands-like C cells of the thyroid (medullary

154 Behavioral, neural, and endocrine habituation to repeated restraint stress and s

155 intermediate markers of cardiometabolic and endocrine health are less established.

156 ure to dLAN has transgenerational effects on endocrine-immune function that may be mediated by global

157 to 50% of patients, generally leading to an endocrine-independent ER+ phenotype.

158 ility and shown to cause regression of a TR, endocrine-independent ER+ xenograft superior to that wit

159 While initial endocrine interventions are successful, resistance to th

160 vity is fundamental to mounting an effective endocrine lineage-specification program within the multi

161 nocopy of menstrual cycle and pregnancy-like endocrine loops and has great potential to be used in dr

162 he in vivo female reproductive tract and the endocrine loops between organ modules for the ovary, fal

163 men network morphogenesis impacts pancreatic endocrine mass.

164 crine progenitor population and, eventually, endocrine mass.

165 Endocrine maturation progresses by up-regulating SUSD2 a

166 ss in wildlife are often limited to baseline endocrine measurements and few have investigated stress

167 tablish biologically plausible links between endocrine mechanisms and apical responses when those end

168 Endocrine mechanisms regulate growth cessation, and thei

169 nd insulation barrier, and secretes numerous endocrine mediators such as adipokines or lipokines.

170 PAC1R) is a potential therapeutic target for endocrine, metabolic and stress-related disorders.

171 host immunity and physiology, including the endocrine, metabolic, and nervous system function in hea

172 SWS is associated with a unique endocrine milieu comprising minimum cortisol and high al

173 ctivity for tumors that develop in different endocrine milieus.

174 ssessments, and without mechanistic data, an endocrine mode of action cannot be determined.

175 emotherapy, supporting the study of adjuvant endocrine monotherapy in this group.

176 Multiple endocrine neoplasia type 2 (MEN 2) syndrome is an autoso

177 cribed as the following phenotypes: multiple endocrine neoplasia type 2A (MEN 2A) and multiple endocr

178 rine neoplasia type 2A (MEN 2A) and multiple endocrine neoplasia type 2B (MEN 2B) syndromes.

179 opment and plasticity in neural, immune, and endocrine networks.

180 function of the central lumen network as an endocrine niche are lacking.

181 ells with ALDH activity can commit to either endocrine or acinar lineages, and can be divided into fo

182 row T-cell hematopoiesis, and extra-skeletal endocrine organ function.

183 Bone has recently emerged as a pleiotropic endocrine organ that secretes at least two hormones, FGF

184 Viewing skeletal muscle as an endocrine organ that secretes various salutary myokines

185 Indeed, the gut microbiome functions like an endocrine organ, generating bioactive metabolites, that

186 recognized as a highly active metabolic and endocrine organ, secreting adipokines that operate as ho

187 also identified developmental changes in the endocrine pancreas of Snord116p-/m+ animals that persist

188 nic development and adult homeostasis of the endocrine pancreas, little is known about what regulates

189 o investigate the role of GATA6 in the adult endocrine pancreas, we generated mice in which Gata6 is

190 eters to assess the functional status of the endocrine pancreas.

191 letal muscle, adipose tissue, brain, and the endocrine pancreas.

192 d cell proliferation, suggesting a potential endocrine/paracrine role for BMPs, but some of the mecha

193 gene approach based on their known roles in endocrine pathways and physiologic processes.

194 couchii evolved by genetic accommodation of endocrine pathways controlling metamorphosis, showing ho

195 BPA disrupts endocrine pathways in fish, but the long-term developmen

196 ed receptors (GPCRs) respond to paracrine or endocrine peptide hormones involved in control of bone h

197 t dedifferentiation/plasticity towards other endocrine phenotypes may play an important role in stres

198 diet-quality scores with cardiometabolic and endocrine plasma biomarkers in US women.

199 of progenitor cells control the size of the endocrine population.

200 ion in adult beta-cells does not involve the endocrine progenitor cell regulator neurogenin3 but requ

201 REAII/-) mice exhibit a massive reduction in endocrine progenitor cells and progeny hormone-producing

202 within already specified Neurog3-expressing endocrine progenitor cells increased the proportion of g

203 Pancreatic endocrine progenitor cells proliferate and transiently e

204 eta cell identity genes and induction of the endocrine progenitor factor neurogenin 3 (NEUROG3).

205 tion factors, specifically in the Neurog3(+) endocrine progenitor lineage (Nkx2.2( big up tri, openen

206 over developmental time and expansion of the endocrine progenitor population and, eventually, endocri

207 s additional essential activities within the endocrine progenitor population.

208 During development, endocrine progenitors delaminate, migrate radially and c

209 ng all four copies of p300/CBP in pancreatic endocrine progenitors failed to establish alpha- and bet

210 Removing p300 in pancreatic endocrine progenitors impaired proliferation of neonatal

211 ion in epithelial multipotent cells, nascent endocrine progenitors, and differentiating and mature be

212 differentiation of Neurogenin3(+) embryonic endocrine progenitors, regardless of the specific endocr

213 on of the alpha-cell-determining Arx gene in endocrine progenitors.

214 Paternal exposure to dLAN decreased splenic endocrine receptor expression and global methylation in

215 Conclusion In endocrine-refractory metastatic breast cancer, Z-endoxif

216 Eligibility included endocrine-refractory, estrogen receptor-positive metasta

217 Prior endocrine regimens during which progression occurred inc

218 Here, we investigated the endocrine regulation of conventional and regulatory T ce

219 ell types through mechanisms of paracrine or endocrine regulation with robust effects on cellular ins

220 nd associated with aggressiveness in various endocrine-related tumors, but its presence, functional r

221 upporting clinical consequences from reduced endocrine reserve.

222 Cytokine activation of ERalpha and endocrine resistance is dependent on phosphorylation of

223 BC either before or after the acquisition of endocrine resistance making functional consequences diff

224 ggest that even following the development of endocrine resistance, ER signaling continues to exert a

225 tion of SOX9 is sufficient to cause relative endocrine resistance.

226 roenvironment controls tumor progression and endocrine resistance.

227 d provide an important resource for studying endocrine resistance.

228 show increased prevalence in the metastatic, endocrine-resistant setting.

229 py is effective in postmenopausal women with endocrine-resistant, hormone receptor-positive and HER2-

230 er CVS would sensitize the behavioral and/or endocrine response to a subthreshold BNST PACAP infusion

231 licited similar but delayed phosphaturia and endocrine responses but did not affect plasma mineral le

232 hway frameworks have diverse applications to endocrine screening and testing.

233 e show that Area II is a primary effector of endocrine-selective transcription in epithelial multipot

234 Nuclear receptors were originally defined as endocrine sensors in humans, leading to the identificati

235 emale D. melanogaster is attributable to the endocrine signal juvenile hormone (JH), which promotes t

236 ings demonstrating that peripherally derived endocrine signals act on receptors in hippocampal neuron

237 The adrenals are a major endocrine site of production/secretion of constitutive p

238 ss be done in every individual fulfilling US Endocrine Society guideline criteria because biochemical

239 the presence of elevated c-Myc and enhances endocrine specification during ductal reprogramming.

240 at the opportunity to individualise adjuvant endocrine strategy accordingly, based on patient prefere

241 of 31 experts from 28 centres, including six endocrine surgeons, used the Delphi method to reach cons

242 n changes.Harmful chemicals that disrupt the endocrine system and hormone regulation have been associ

243 The endocrine system dynamically controls tissue differentia

244 regard, the neural mechanisms by which this endocrine system may impact stress-related pathologies a

245 ffects to the testis and to the reproductive endocrine system that persisted long-term.

246 crine disrupting chemicals in the developing endocrine system.

247 oxifen injection on the testis and the wider endocrine system.

248 uires precise coordination between different endocrine systems and multiple organs.

249 e, respiratory, gastrointestinal, liver, and endocrine systems, by influencing cellular signaling pat

250 changes are orchestrated by the nervous and endocrine systems.

251 Although second generation endocrine therapies have significantly improved survival

252 describe benefits and toxicities of adjuvant endocrine therapies in women younger than 35 years with

253 s for estrogen has led to the development of endocrine therapies that block the action of these hormo

254 Endocrine therapies that target the dependence of this s

255 re found in >20% of tumours that progress on endocrine therapies.

256 s studies suggest that adherence to adjuvant endocrine therapy (AET) for patients with breast cancer

257 monstrated the clinical benefits of adjuvant endocrine therapy (AET) in preventing recurrence and dea

258 dy Group, was stratified by type of previous endocrine therapy (aromatase inhibitors only vs selectiv

259 own about the efficacy of the combination of endocrine therapy (ET) with trastuzumab or with the pote

260 sly demonstrated that a switch from adjuvant endocrine therapy after 2 to 3 years of tamoxifen to exe

261 breast cancer, who had relapsed on or after endocrine therapy and mTOR inhibitors, were recruited fr

262 than 35 years stopped all protocol-assigned endocrine therapy early.

263 od or who underwent radical prostatectomy or endocrine therapy exhibited slightly lower HRs for prost

264 The administration of endocrine therapy for 5 years substantially reduces recu

265 Endocrine therapy given for 5-10 y after surgery improve

266 The estrogen receptor (ER) is a target for endocrine therapy in breast cancer patients.

267 ationale for the use of PI3K inhibitors plus endocrine therapy in patients with PIK3CA mutations.

268 xemestane are reasonable options as adjuvant endocrine therapy in postmenopausal patients with hormon

269 tudy show that PI3K inhibition combined with endocrine therapy is effective in postmenopausal women w

270 If adjuvant endocrine therapy is indicated for breast cancer treatme

271 lesterol-lowering medication during adjuvant endocrine therapy may have a role in preventing breast c

272 Resistance to endocrine therapy remains a major clinical problem in br

273 nduced cancer stem-like cells and leading to endocrine therapy resistance in OXPHOS-dependent breast

274 ween IL-6 and STAT3 driving tumor growth and endocrine therapy resistance.

275 sm for altering cell signaling and acquiring endocrine therapy resistance.

276 naling is affected by genetic alterations in endocrine therapy resistance.

277 d at least partly explained by the advent of endocrine therapy that is less effective in African Amer

278 ositive breast cancers develop resistance to endocrine therapy via mutation of ERs whose constitutive

279 ast cancer cells often develop resistance to endocrine therapy via restoration of the ERalpha activit

280 Initiation of CLM during endocrine therapy was related to improved disease-free-s

281 An alternative schedule of extended adjuvant endocrine therapy with letrozole, including intermittent

282 noma, had completed treatment (not including endocrine therapy) 2 months to 5 years previously, were

283 ive breast cancers following radiotherapy or endocrine therapy, and this drives tumorigenesis and the

284 After 5 years of adjuvant endocrine therapy, breast-cancer recurrences continued t

285 tive breast cancer are treated with adjuvant endocrine therapy, including selective estrogen receptor

286 ined as imaging surveillance with or without endocrine therapy, vs standard surgical care.

287 mine whether patients should be treated with endocrine therapy, which is designed to block ERalpha si

288 of having a toolkit of AEs for treatment of endocrine therapy-resistant tumors driven by different c

289 apy) and had completed 4-6 years of adjuvant endocrine therapy.

290 uently in breast cancer that is resistant to endocrine therapy.

291 ve breast cancers undergoing radiotherapy or endocrine therapy.

292 erapy, postmastectomy radiation therapy, and endocrine therapy.

293 alpha gene expression is a critical topic of endocrine therapy.

294 can occur despite appropriate treatment with endocrine therapy.

295 receptor-positive breast cancer who received endocrine therapy.

296 breast cancers and is the primary target of endocrine therapy.

297 ) remains a major challenge in breast cancer endocrine therapy.

298 plasticity under the control of hormones and endocrine therapy.

299 t cancer and the mechanisms of resistance to endocrine therapy.

300 geted therapies that enhance the efficacy of endocrine therapy; inhibitors of mTOR and inhibitors of